Proteomics

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4E-BP1 counteracts human stem cell senescence via maintaining mitochondrial homeostasis

ABSTRACT: Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders, the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown. Here, we report that the expression of 4E-BP1 decreases along with the senescence of human mesenchymal stem cells (hMSCs). Genetic inactivation of 4E-BP1 in hMSCs accelerates cellular senescence, compromises mitochondrial respiration and increases mitochondrial ROS production. Mechanistically, the absence of 4E-BP1 destabilizes proteins in mitochondrial respiration complexes, especially several key subunits of the complex III including UQCRC2. Ectopic expression of 4E-BP1 attenuates mitochondrial abnormalities and alleviates cellular senescence in 4E-BP1-deficient hMSCs as well as in physiologically aged hMSCs. These findings together demonstrate that 4E-BP1 functions as a geroprotector to alleviate human stem cell senescence and maintain mitochondrial homeostasis, particularly for the mitochondrial respiration complex III and provide a new potential target to counteract human stem cell senescence.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Stem Cell, Cell Culture

SUBMITTER: ji zhao  

LAB HEAD: Qianzhao Ji

PROVIDER: PXD033301 | Pride | 2023-05-10

REPOSITORIES: Pride

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4E-BP1 counteracts human mesenchymal stem cell senescence via maintaining mitochondrial homeostasis.

He Yifang Y   Ji Qianzhao Q   Wu Zeming Z   Cai Yusheng Y   Yin Jian J   Zhang Yiyuan Y   Zhang Sheng S   Liu Xiaoqian X   Zhang Weiqi W   Liu Guang-Hui GH   Wang Si S   Song Moshi M   Qu Jing J  

Protein & cell 20230401 3

Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders, the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown. Here, we report that the expression of 4E-BP1 decreases along with the senescence of human mesenchymal stem cells (hMSCs). Genetic inactivation of 4E-BP1 in hMSCs compromises mitochondrial respiration, increases mitochondrial reactive oxygen species (ROS) production, and accelerates cellular senescence. Mechanisticall  ...[more]

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